Naltrexone has the chemical name morphinan-6-one, 17-(cyclopropylmethyl)-4,5-epoxy-3,14-dihydroxy-(5α). The molecular formula of naltrexone is C20H23NO4 and its molecular weight is 341.41 in the anhydrous form (<1% maximum water content). The chemical structure of naltrexone is shown below.

Naltrexone has been approved for use in the treatment of alcoholism or narcotic addiction. It is believed that naltrexone functions by blocking the brain receptors that trigger the effects of alcohol or narcotics. Naltrexone is marketed by Durmed in the form of a tablet under the tradename ReVia® and by Alkermes in the form of a powder for injectable suspension under the tradename Vivitrol®.
Naloxone has the chemical name (−)-17-allyl-4,5α-epoxy-3,14-dihydroxymorphinan-6-one and the molecular formula C19H21NO4. The chemical structure of naloxone is shown below.

Naloxone is typically administered intravenously because of its short duration of action, and is generally administered to a patient in order to reverse opioid depression, including respiratory depression, induced by natural and synthetic opioids.
Nalmefene has the chemical name 17-cyclopropylmethyl-4,5α-epoxy-6-methylenemorphinan-3,14-diol and the molecular formula C21H25NO3. The chemical structure of nalmefene is shown below.

Nalmefene is typically used in the management of alcohol dependence, and also has been investigated for the treatment of other addictions such as pathological gambling and addiction to shopping. Advantages of nalmefene relative to naltrexone include longer half-life, greater oral bioavailability and no observed dose-dependent liver toxicity. As with other drugs of this type, nalmefene can precipitate acute withdrawal symptoms in patients who are dependent on opioid drugs, or more rarely when used post-operatively to counteract the effects of strong opioids used in surgery.
In the early 1980s, it was reported that the administration of low dose naltrexone (less than 10 mg naltrexone per day) increases the production of endogenous endomorphins, especially the endogenous pentapeptide metenkephalin, and increases the number and density of metenkephalin receptors by intermittently blocking opiate receptors. (I. S. Zagon & P. J. McLaughlin, “Naltrexone modulates tumor response in mice with neuroblastoma”, Science, 221: 671-3 (12 Aug. 1983). This increase in metenkephalin is believed to enhance homeostatic regulation of the natural immune function of the human body.
In view of Zagon's findings, Bernard Bihari reported the use of low dose naltrexone for the treatment of patients with AIDS (U.S. Pat. No. 4,888,346) and herpes (U.S. Pat. No. 5,356,900). Further, Nicholas Plotnikoff reported the use of low dose naltrexone for the treatment of herpes, HIV infection, cytomegalovirus, coronavirus, influenza A and Japanese encephalitis. (E. A. Moore & S. Wilkinson, THE PROMISE OF LOW DOSE NALTREXONE THERAPY: POTENTIAL BENEFITS IN CANCER, AUTOIMMUNE, NEUROLOGICAL AND INFECTIOUS DISORDERS (McFarland & Company, Inc., Publishers, 2009)).
Herpes zoster (or shingles) is a disease caused by the reactivation of the varicella-zoster virus (VZV). The VZV causes chickenpox (or varicella) generally during childhood and can lie in a dormant state in nerve cells along the spine afterwards. The VZV can re-emerge later as shingle, most commonly in adults, especially those over the age of 60 or those with weak immune systems. One of the major symptoms of shingles is a unilateral vesicular eruption with dermatomal distribution. The onset of the disease is often preceded by pain 48 to 72 hours before the rash develops in the affected dermatome. The rash may appear as erythematous, maculopapular lesions that rapidly evolve into vesicles. The vesicles may coalesce and form bullous lesions. The lesions may continue to form for 3 to 5 days, with a total duration of the disease of 10 to 15 days. However it can take as long as 1 month before the skin returns to normal.
Herpes zoster can also affect the surrounding regions of the eye and the eye itself. This is called herpes zoster ophthalmicus—the reactivation of a varicella-zoster virus infection involving the eye. Symptoms and signs, which may be intense, include dermatomal forehead rash and painful inflammation of all the tissues of the anterior and, rarely, posterior structures of the eye. Complications may include: keratitis accompanied by uveitis; late sequelae, such as glaucoma, cataract, chronic or recurrent uveitis, corneal scarring, corneal neovascularization, or hypesthesia; and postherpetic neuralgia. (Herpes zoster opthalmicus, The Merck manual of diagnosis and therapy, The Merck manuals online medical library. http://www.merck.com/mmpe/sec09/ch102/ch102e.html#sec09-ch102-ch102e-355, Accessed Jan. 6, 2010). Current treatments for herpes zoster include topical, oral, or ophthalmic administration of an antiviral agent, such as acyclovir, valacyclovir or famciclovir.